3203Pure, White And Deadly: How sugar is killing us and what we can do to stop it Pure, White And Deadly: How sugar is killing us and what we can do to stop it Pure, White And Deadly: How sugar is killing us and what we can do to stop it John Yudkin19/12/2012
Hear from the author's son, Professor Michael Yudkin, and US obesity expert Professor Robert Lustig - whose recent work has rekindled interest in the dangers of sugar - at either of two special events hosted by FAB Research, aimed at policymakers, professionals and the general public.
Sugar. It's killing us. Why do we eat so much of it? What are its hidden dangers?
In 1972, when British scientist John Yudkin first proved that sugar was bad for our health, he was ignored by the majority of the medical profession and rubbished by the food industry. We should have heeded his warning.
Today, 1 in 4 adults in the UK are overweight
There is an epidemic of obese six month olds around the globe
Sugar consumption has tripled since World War II
Using everyday language and a range of scientific evidence, Professor Yudkin explores the ins and out of sugar, from the different types - is brown sugar really better than white? - to how it is hidden inside our everyday foods, and how it is damaging our health.
Brought up-to-date by childhood obesity expert Dr Robert Lustig M.D., his classic exposé on the hidden dangers of sugar is essential reading for anyone interested in their health, the health of their children and the health of modern society.
'Arguably the leading nutritionist of his time' Guardian
'Yudkin was far ahead of his time with his idea of nutrition as a subject of great breadth: not just the study of the composition of foods, but the importance of enjoying a variety of fresh foods, and the recognition of the psychological and social factors that cause us to choose certain foods and avoid others' Independent
'Worldwide, around 180million tonnes of refined sugar is produced each year and the UK market alone is worth nearly £1billion. Little wonder that no one listened to eminent nutritionist Professor John Yudkin when he called sugar 'pure, white and deadly' back in 1972 and quite rightly warned of the links between excessive consumption and heart disease' Catherine Collins, Principal Dietician, St George's Hospital
John Yudkin (8 August 1910 - 12 July 1995) was a British physiologist and nutritionist, whose books include This Slimming Business, Eat Well, Slim Well and This Nutrition Business. He became internationally famous with his book Pure, White and Deadly, first published in 1972, and was one of the first scientists to claim that sugar was a major cause of obesity and heart disease.
Robert H. Lustig, M.D. has spent the past sixteen years treating childhood obesity and studying the effects of sugar on the central nervous system and metabolism. He is the Director of the UCSF Weight Assessment for Teen and Child Health Program and also a member of the Obesity Task Force of the Endocrine Society. His YouTube video lecture Sugar: The Bitter Truth has received over two million hits, he recently appeared on the BBC 2 documentary The Men Who Made Us Fat and his book Fat Chance: Beating the Odds Against Sugar, Processed Food, Obesity, and Disease is being published in January 2013.
Sugar, glucose, fructose, refined sugar, Pure, White and Deadly.jpgPure, White and Deadlyhttp://www.amazon.co.uk/exec/obidos/ASIN/0241965284/fabresearfood-21http://www.amazon.com/exec/obidos/ASIN/0241965284/fabresearch-20
324912 Dec 2012 - MedicalXpress - Could ending your fatty food habit cause withdrawal symptoms and depression?Could ending your fatty food habit cause withdrawal symptoms and depression?12/12/2012
Even before obesity occurs, eating fatty and sugary foods causes chemical changes in the brain, meaning that going on a diet might feel similar to going through drug withdrawal, according to a study published today by Dr. Stephanie Fulton of the University of Montreal's Faculty of Medicine and its affiliated CRCHUM Hospital Research Centre.
"By working with mice, whose brains are in many ways comparable to our own, we discovered that the neurochemistry of the animals who had been fed a high fat, sugary diet were different from those who had been fed a healthy diet," Fulton explained.
"The chemicals changed by the diet are associated with depression. A change of diet then causes withdrawal symptoms and a greater sensitivity to stressful situations, launching a vicious cycle of poor eating."
The research team feed one group of mice a low-fat diet and a high fat diet to a second group over six weeks, monitoring how the different food affected the way the animals behave. Fat represented 11% of the calories in the low-fat diet and 58% in the high-fat diet, causing the waist size in the latter group to increase by 11% – not yet obese. Next, Fulton and her colleagues use a variety of scientifically validated techniques to evaluate the relationship between rewarding mice with food and their resulting behaviour and emotions.
They also actually looked at the brains of the mice to see how they had changed. Mice that had been fed the higher-fat diet exhibited signs of being anxious, such as an avoidance of open areas. Moreover, their brains have been physically altered by their experiences.
One of molecules in the brain that the researchers looked at is dopamine. It enables the brain to rewards us with good feelings, thereby encouraging us to learn certain kinds of behaviour. This chemical is the same in humans as it is in mice and other animals. In turn, CREB is a molecule that controls the activation of genes involved in the functioning of our brains, including those that cause the production of dopamine. It contributes to memory formation.
"CREB is much more activated in the brains of higher-fat diet mice and these mice also have higher levels of corticosterone, a hormone that is associated with stress. This explains both the depression and the negative behaviour cycle," Fulton said.
"It's interesting that these changes occur before obesity. These findings challenge our understanding of the relationship between diet, the body and the mind. It is food for thought about how we might support people psychologically as they strive to adopt healthy eating habits, regardless of their current corpulence."
3248Sharma et al 2012 - Adaptations in brain reward circuitry underlie palatable food cravings and anxiety induced by high-fat diet withdrawal.Adaptations in brain reward circuitry underlie palatable food cravings and anxiety induced by high-fat diet withdrawal.Adaptations in brain reward circuitry underlie palatable food cravings and anxiety induced by high-fat diet withdrawal.Sharma S, Fernandes MF, Fulton S.11/12/2012Int J Obes (Lond). Dec 11. doi: 10.1038/ijo.2012.197. [Epub ahead of print]
To identify the emotional and motivational processes that reinstate palatable food intake following removal of high-fat diet (HFD) and associated neuroadaptations tied to neurochemical and behavioural changes underlying dopaminergic function.
Adult male C57Bl6 mice were placed on a HFD (58% kcal fat) or ingredient-matched, low-fat diet (LFD; 11% kcal fat) for 6 weeks. At the end of diet-regimen mice were either maintained on their respective diets, or HFD and LFD were replaced with normal chow (withdrawal). Effort-based operant responding for sucrose and high-fat food rewards was measured along with basal and stress-induced corticosterone levels and anxiety (elevated-plus maze). Protein levels for tyrosine hydroxylase (TH), corticosterone releasing factor type 1 receptor (CRF-R1), brain-derived neurotrophic factor (BDNF), phospho-CREB (pCREB) and ΔFosB (truncated splice variant of FosB) were assessed in the amygdala, nucleus accumbens (NAc) and ventral tegmental area (VTA) via western immunoblotting.
Six weeks of HFD resulting in significant weight gain elicited sucrose anhedonia, anxiety-like behaviour and hypothalamic-pituitary-adrenocortical axis (HPA) hypersensitivity to stress. Withdrawal from HFD but not LFD-potentiated anxiety and basal corticosterone levels and enhanced motivation for sucrose and high-fat food rewards. Chronic high-fat feeding reduced CRF-R1 and increased BDNF and pCREB protein levels in the amygdala and reduced TH and increased ΔFosB protein in NAc and VTA. Heightened palatable food reward in mice withdrawn from HFD coincided with increased BDNF protein levels in NAc and decreased TH and pCREB expression in the amygdala.
Anhedonia, anxiety and sensitivity to stressors develops during the course of HFD and may have a key role in a vicious cycle that perpetuates high-fat feeding and the development of obesity. Removal of HFD enhances stress responses and heightens vulnerability for palatable foods by increasing food-motivated behaviour. Lasting changes in dopamine and plasticity-related signals in reward circuitry may promote negative emotional states, overeating and palatable food relapse.
obesity, diet, depression, anhedonia, withdrawal, substance dependence, mechanisms, animal study, experimental studyhttp://www.ncbi.nlm.nih.gov/pubmed/23229740View this and related abstracts via PubMed here
3699McCaddon 2013 - Vitamin B12 in neurology and ageing; clinical and genetic aspectsVitamin B12 in neurology and ageing; clinical and genetic aspectsVitamin B12 in neurology and ageing; clinical and genetic aspectsMcCaddon A.07/12/2012Biochimie95(5):1066-76. Epub 2012 Dec 7.
The classic neurological and psychiatric features associated with vitamin B12 deficiency have been well described and are the subject of many excellent review articles.
The advent of sensitive diagnostic tests, including homocysteine and methylmalonic acid assays, has revealed a surprisingly high prevalence of a more subtle 'subclinical' form of B12 deficiency, particularly within the elderly.
This is often associated with cognitive impairment and dementia, including Alzheimer's disease. Metabolic evidence of B12 deficiency is also reported in association with other neurodegenerative disorders including vascular dementia, Parkinson's disease and multiple sclerosis.
These conditions are all associated with chronic neuro-inflammation and oxidative stress. It is possible that these clinical associations reflect compromised vitamin B12 metabolism due to such stress.
Physicians are also increasingly aware of considerable inter-individual variation in the clinical response to B12 replacement therapy. Further research is needed to determine to what extent this is attributable to genetic determinants of vitamin B12 absorption, distribution and cellular uptake.
Vit_B12, neurology, psychiatry, dementia, Alzheimer's, Parkinson's, neurodegenerative disorders, oxidative stress, reviewhttp://www.ncbi.nlm.nih.gov/pubmed/23228515View this and related abstracts via PubMed here.
3653Ming et al 2013 - Metabolic perturbance in autism spectrum disorders: a metabolomics studyMetabolic perturbance in autism spectrum disorders: a metabolomics studyMetabolic perturbance in autism spectrum disorders: a metabolomics study
Ming X, Stein TP, Barnes V, Rhodes N, Guo L07/12/2012J Proteome Res. 2012 Dec 7;11(12):5856-62. doi: 10.1021/pr300910n
Autism spectrum disorders (ASD) are a group of biological disorders with associated metabolic derangement. This study aimed to identify a pattern of metabolic perturbance in ASD using metabolomics in urinary specimens from 48 children with ASD and 53 age matched controls. Using a combination of liquid- and gas-chromatography-based mass spectrometry, we detected the levels of 82 metabolites (53 of which were increased) that were significantly altered between the ASD and the control groups using osmolality normalized data. Pattern analysis showed that the levels of several amino acids such as glycine, serine, threonine, alanine, histidine, glutamyl amino acids and the organic acid, taurine were significantly (p≤0.05) lower in ASD children. The levels of antioxidants such as carnosine were also reduced in ASD (p=0.054). Furthermore, several gut bacterial metabolites were significantly altered in ASD children who had gastrointestinal dysfunction. Overall, this study detected abnormal amino acid metabolism, increased oxidative stress, and altered gut microbiomes in ASD. The relationship of altered gut microbial co-metabolism and the disrupted metabolisms requires further investigation.
Autism spectrum disorders; metabolomics; gut bacteria; metabolic perturbanceautism spectrum disorders; metabolomics; gut bacteria; metabolic perturbanceView this and related abstracts via PubMed here
32014 Dec 2012 - BBC News - 'Binge-drinking gene' discoveredbinge-drinking geneScientists believe some people have a gene that hard-wires them for binge drinking by boosting levels of a happy brain chemical triggered by alcohol.04/12/2012
The gene - RASGRF-2 - is one of many already suggested to be linked with problem drinking, PNAS journal reports.
The King's College London team found animals lacking the gene had far less desire for alcohol than those with it.
Brain scans of 663 teenage boys showed those with a version of the gene had heightened dopamine responses in tests.
During a task designed to make them anticipate a reward, these 14-year-old boys had more activity in a part of the brain called the ventral striatum which is known to be involved in dopamine release.
When the researchers later contacted the same boys at the age of 16 and asked them about their drinking habits, they found the boys with the 'culprit' variation on the RASGRF-2 gene drank more frequently.
Binge-drinking usually refers to drinking lots of alcohol in a short space of time or drinking to get drunk, that’s eight or more units in a single session for men and six or more for women.
However, according to researchers, this definition does not apply to everyone because the tolerance and the speed of drinking in a session varies from person to person.
Binge-drinking increases the risk of heart attack. It could cause you to vomit and if you’re sick when very drunk you could breathe in your own vomit and suffocate.
For more information on binge-drinking and current recommendations, visit NHS Choices.
http://www.bbc.co.uk/news/health-20583113?utm_source=Email+Campaign&utm_medium=email&utm_campaign=283098-NH-eNews+-+December+4th+2012+Read the full news item and related stories on the BBC News website here
321626 Nov 2012 - BBC News - How we became addicted to sugarhow we became addicted to sugarWe are swamped by sugar. It has crept into all areas of our daily diet, from the sweet treats we award ourselves to family essentials such as pre-packaged loaves of bread.26/11/2012
We know that too much sugar is bad for us, but we are hooked - and sugar is now so ubiquitous it is hard to believe there was a time when it was not readily available.
Sugar is now so ingrained in our diet it may seem too impossible a habit to break. But Professor Naveed Sattar of the University of Glasgow's School of Medicine thinks there is some hope in our battle with the sweet stuff.
"People can take some of the sugar out of their diet and get to a point where they're eating less sugar in their food or drinks but still enjoy their diet to the same extent, if not more, by reprogramming their palate."
Challenging centuries of in-built programming favouring sugar might take a lot of willpower, but Professor Sattar is confident it can be achieved.
"Sometimes to re-programme your palate can take a couple of months… but people can achieve that change."
Continue reading this interesting and enlightening article about the history of sugar, how it reached our shores, and found it's way into the family diet to become a household favourite, on the BBC website at the link below.
http://www.bbc.co.uk/history/0/20311399Read the full article on the BBC website here
319922 Nov 2012 - Nutraingredients - Preventing malnutrition will save money as well as lives, says the UNPreventing malnutrition will save money as well as lives, says the UNInvestment in battling malnutrition on a global scale will help save and improve millions of lives, but will also save billions of euros on lost potential GDP for countries where malnutrition is a problem, according to the United Nations 22/11/2012by Nathan Gray
Malnutrition is a global problem that leads to stunted growth and the wasting of bodily tissues. Yet for a relatively small investment, the problem of malnutrition, and all of the issues that accompany it, could be resolved.
Stunting imposes an enormous cost on individuals and economies in terms of mortality, morbidity, loss of productivity and choronic disease. Read the full article and more on:
The problem of stunting
A lifetime of trouble
An economic problem?
http://www.nutraingredients.com/Industry/Preventing-malnutrition-will-save-money-as-well-as-lives-says-the-UNRead the full news article on Nutraingredients here
3485Nilsson et al 2012 - Effects of supplementation with n-3 PUFA on cognitive performance and cardiometabolic risk markers in healthy adults aged 51-72 years: a RCTEffects of supplementation with n-3 polyunsaturated fatty acids on cognitive performance and cardiometabolic risk markers in healthy 51 to 72 years old subjects: a randomized controlled cross-over study.Effects of supplementation with n-3 polyunsaturated fatty acids on cognitive performance and cardiometabolic risk markers in healthy 51 to 72 years old subjects: a randomized controlled cross-over study.Nilsson A, Radeborg K, Salo I, Björck I.22/11/2012Nutr J. 1199. doi: 10.1186/1475-2891-11-99.
Higher plasma n-3 polyunsaturated fatty acids (PUFA) have been associated with a lower risk of age related cognitive decline, and to beneficially affect cardiometabolic risk factors. A relation exists between metabolic disorders such as diabetes type 2 and cognitive decline. Results regarding the potential effects of n-3 PUFA on risk factors in healthy subjects are divergent, and studies regarding the possible relation between cardiometabolic parameters and cognitive performance are scarce. The objective was to evaluate the effects of five weeks intake of long chain n-3 PUFA on cognitive performance in healthy individuals, and to exploit the possible relation between outcomes in cognitive tests to cardiometabolic risk parameters.
Fish oil n-3 PUFA (3g daily) were consumed during 5 weeks separated by a 5 week washout period in a cross-over placebo controlled study, including 40 healthy middle aged to elderly subjects. Cognitive performance was determined by tests measuring working memory (WM) and selective attention.
Supplementation with n-3 PUFA resulted in better performance in the WM-test compared with placebo (p < 0.05). In contrast to placebo, n-3 PUFA lowered plasma triacylglycerides (P < 0.05) and systolic blood pressure (p < 0.0001). Systolic blood pressure (p < 0.05), f-glucose (p = 0.05), and s-TNF-α (p = 0.05), were inversely related to the performance in cognitive tests.
Intake of n-3 PUFA improved cognitive performance in healthy subjects after five weeks compared with placebo. In addition, inverse relations were obtained between cardiometabolic risk factors and cognitive performance, indicating a potential of dietary prevention strategies to delay onset of metabolic disorders and associated cognitive decline.
omega-3, cognition, cardiovascular health, older adults, human study, intervention study, RCThttp://www.ncbi.nlm.nih.gov/pubmed/23173831View this and related abstracts via PubMed here. Free full text of this article is available online.
320021 Nov 2012 - Nutraingredients - Study calls for maternal vitamin D supplementationMaternal vitamin D supplementationNew data that strongly implicates maternal levels of vitamin D with the risk of multiple sclerosis (MS) in children means there is now a strong case for supplementation in pregnant women in countries where sunlight levels are low between October and March21/11/2012by Nathan Gray
The systematic review of previous studies in this area - published in the Journal of Neurology Neurosurgery and Psychiatry - finds that the month a child is born in has a significant effect on subsequent risk of developing MS.
Led by Dr Ruth Dobson from Queen Mary University of London, UK, the study finds that risk of babies developing MS is highest in the month of April, and lowest in October.
"This is likely to be due to ultraviolet light exposure and maternal vitamin D levels, as demonstrated by the relationship between risk and latitude," write Dobson and her colleagues.
This systematic review shows a significant association between multiple sclerosis and month of birth, with children born in April being at highest risk, and those born in October at lowest risk. Data on over 150,000 patients with MS were included in this meta-analysis, so these findings appear very robust.
Maternal Vitamin D deficiency during pregnancy is the key factor that can account for this link - because exposure of the skin to strong sunshine is the main source of Vitamin D. In countries at latitudes like the UK, Northern America and Canada, or Scandinavia, no Vitamin D can be made during the winter months.
Deficiencies of Vitamin D are known to be widespread in the general population in the UK and many other countries. These results again raise the question of just how much more evidence is needed of the damaging effects of Vitamin D deficiency in pregnancy before some effective public health measures are taken - such as following the authors' call for Vitamin D supplementation of all pregnant mothers.
319620 Nov 2012 - Nutraingredients - Maternal vitamin C backed for baby's brain developmentVitamin C deficiency, pregnancy, brain development, nutritional programming20/11/2012By Nathan Gray
Maternal deficiency in vitamin during pregnancy could have serious consequences for the development of the foetal brain that cannot be reversed, according to new research data.
A lack of vitamin C during pregnancy can have serious consequences for the development of the foetal brain, leading to long term damage that cannot be reversed after birth, warn researchers writing in PLoS ONE.
"Even marginal Vitamin C deficiency in the mother stunts the foetal hippocampus, the important memory centre, by 10-15%, preventing the brain from optimal development", said research leader Professor Jens Lykkesfeldt - from the University of Copenhagen, Denmark.
Even mild deficiencies of Vitamin C in pregnant mothers can permanently impair the brain development of their unborn children, according to this animal study.
The same researchers have already shown that Vitamin C deficiency led to memory problems in newborns (see Tveden-Nyborg et al 2009) And the brain areas affected by maternal Vitamin C deficiency in this study are well known to support memory functions.
These findings have very serious implications if they can be generalised to humans. Of course experimental studies like this can never be done in humans for ethical reasons (but guinea pigs provide a good model, because like humans, they cannot make Vitamin C). However, these results are of sufficient concern that they deserve urgent investigation, and existing datasets from large birth cohort studies could be used to address the key question:
- Is low Vitamin C status in pregnant mothers really associated with lifelong memory deficits in the resulting offspring?
3197Tveden-Nyborg et al 2012 - Maternal Vitamin C Deficiency during Pregnancy Persistently Impairs Hippocampal Neurogenesis in Offspring of Guinea PigsMaternal Vitamin C Deficiency during Pregnancy Persistently Impairs Hippocampal Neurogenesis in Offspring of Guinea PigsMaternal Vitamin C Deficiency during Pregnancy Persistently Impairs Hippocampal Neurogenesis in Offspring of Guinea Pigs
Tveden-Nyborg P, Vogt L, Schjoldager JG, Jeannet N, Hasselholt S, Paidi MD, Christen S, Lykkesfeldt J20/11/2012doi: 10.1371/journal.pone.0048488
While having the highest vitamin C (VitC) concentrations in the body, specific functions of VitC in the brain have only recently been acknowledged.
We have shown that postnatal VitC deficiency in guinea pigs causes impairment of hippocampal memory function and leads to 30% less neurons. This study investigates how prenatal VitC deficiency affects postnatal hippocampal development and if any such effect can be reversed by postnatal VitC repletion.
Eighty pregnant Dunkin Hartley guinea pig dams were randomized into weight stratified groups receiving High (900 mg) or Low (100 mg) VitC per kg diet. Newborn pups (n = 157) were randomized into a total of four postnatal feeding regimens: High/High (Control); High/Low (Depleted), Low/Low (Deficient); and Low/High (Repleted).
Proliferation and migration of newborn cells in the dentate gyrus was assessed by BrdU labeling and hippocampal volumes were determined by stereology.
Prenatal VitC deficiency resulted in a significant reduction in postnatal hippocampal volume (P<0.001)
There was no difference in postnatal cellular proliferation and survival rates in the hippocampus between dietary groups, however, migration of newborn cells into the granular layer of the hippocampus dentate gyrus was significantly reduced in prenatally deficient animals (P<0.01).
We conclude that a prenatal VitC deficiency in guinea pigs leads to persistent impairment of postnatal hippocampal development which is not alleviated by postnatal repletion. Our findings place attention on a yet unrecognized consequence of marginal VitC deficiency during pregnancy.
brain function; vitamin C, brain development, pregnancy, diet, nutritional programming, animal study, experimental studyhttp://www.ncbi.nlm.nih.gov/pubmed/23119033View this and related abstracts via PubMed here. Free full text of this article is available online.
319518 Nov 2012 - The Guardian - Britain in nutrition recession as food prices rise and incomes shrinknutrition recessionFamilies filling up on high-fat processed foods as 900,000 fewer in two years manage 'five-a-day' fruit and vegetables18/11/2012By Patrick Butler
Austerity Britain is experiencing a nutritional recession, with rising food prices and shrinking incomes driving up consumption of fatty foods, reducing the amount of fruit and vegetables we buy, and condeming people on the lowest incomes to an increasingly unhealthy diet.
Detailed data compiled for the Guardian, which analysed the grocery buying habits of thousands of UK citizens, shows that consumption of fat, sugar and saturates has soared since 2010, particularly among the poorest households, despite the overall volume of food bought remaining almost static. Food experts and campaigners called for government action to address concerns the UK faces a sustained nutritional crisis triggered by food poverty, which is in turn storing up public health problems that threaten to widen inequalities between rich and poor households.
http://www.guardian.co.uk/society/2012/nov/18/breadline-britain-nutritional-recession-austerity?INTCMP=SRCHRead the full news item in The Guardian here
3245Dobson et al 2012 - The month of birth effect in multiple sclerosis: systematic review, meta-analysis and effect of latitude.The month of birth effect in multiple sclerosis: systematic review, meta-analysis and effect of latitude.The month of birth effect in multiple sclerosis: systematic review, meta-analysis and effect of latitude.Dobson R, Giovannoni G, Ramagopalan S.14/11/2012J Neurol Neurosurg Psychiatry. Nov 14. [Epub ahead of print]
Month of birth has previously been described as a risk factor for multiple sclerosis (MS). This has been hypothesised to be related to maternal vitamin D levels during pregnancy, although conclusive evidence to support this is lacking. To date, no large studies of latitudinal variation in the month of birth effect have been performed to advance this hypothesis.
Previously published data on month of birth from 151 978 MS patients were compared to expected birth rates. A linear regression model was used to assess the relationship between latitude and observed:expected birth ratio of MS patients for each month.
Analysis of all reported data demonstrated a significant excess of MS risk in those born in April (observed:expected 1.05, p=0.05) and reduction in risk in those born in October (0.95, p=0.04) and November (0.92 p=0.01). A conservative analysis of 78 488 patients revealed an excess MS risk in those born in April (1.07, p=0.002) and May (1.11, p=0.0006), and a reduced risk in those born in October (ratio 0.94, p=0.004) and November (0.88, p=0.0002). A significant relationship between latitude and observed:expected ratio was demonstrated in December, and borderline significant relationships in May and August.
Month of birth has a significant effect on subsequent MS risk. This is likely to be due to ultraviolet light exposure and maternal vitamin D levels, as demonstrated by the relationship between risk and latitude.
Vitamin_D, Vit_D, neurological disorders, Multiple Sclerosis, human study, population study, season of birth, systematic review, meta-analysishttp://www.ncbi.nlm.nih.gov/pubmed/23152637View this and related abstracts via PubMed here
31949 Nov 2012 - Psych Central - The Gluten-Mood Connectiongluten freeInformation about why doing a Gluten-Free Challenge may be right for you.09/11/2012By Trudy Scott
There are many studies supporting the gluten-mood connection – anxiety, social phobia, depression and even schizophrenia. A 2002 study titled Psychiatric Symptoms and Celiac Disease states that celiac disease “should be taken into consideration in patients with psychiatric disorders particularly if you are not responsive to psycho-pharmacological therapy, because withdrawal of gluten from the diet usually results in disappearance of symptoms.”
Gluten can also cause fatigue, aches and pains, poor focus and of course digestive problems like constipation, gas, diarrhea and bloating, and these symptoms.
Trudy Scott works with women with mood problems and assesses all her clients for gluten intolerance, and most of them do experience dramatic improvements on a gluten-free diet – improved mood, no more anxiety, more energy, better sleep and improved digestion.
319029 Oct 2012 - D is for Dementia - Vitamin D and Brain HealthVitamin D,cognition and dementiaThink of the health benefits of vitamin D, and you’ll probably think of bone strength. For decades, diseases like osteoporosis, osteopenia, and osteomalacia have been prevented and treated with adequate vitamin D intake, among other interventions. In recent years, the evidence that vitamin D affects more than just bones has mounted; cardiovascular disease, cancers, stroke, depression, and metabolic disorders have all been linked to low vitamin D levels. A new review adds cognitive decline and dementia to that list.29/10/2012By Jennifer Gibson
The authors of a new review assessed 37 studies that evaluated vitamin D concentrations and cognitive function. The studies included various populations and age groups, but most included both men and women over 65 years of age. As part of the review, the authors conducted two meta-analyses: one to compare the mean vitamin D concentration between participants with Alzheimer’s disease (AD) and controls and one to compare mean mental status scores between participants with low vitamin D levels and those with higher levels.
318825 Oct 2012 - MedicalXpress - Omega-3 intake heightens working memory in healthy young adultsomega-3 and working memory26/10/2012
While Omega-3 essential fatty acids—found in foods like wild fish and grass-fed livestock—are necessary for human body functioning, their effects on the working memory of healthy young adults have not been studied until now.
In the first study of its kind, researchers at the University of Pittsburgh have determined that healthy young adults ages 18-25 can improve their working memory even further by increasing their Omega-3 fatty acid intake. Their findings have been published online in PLOS One.
"Before seeing this data, I would have said it was impossible to move young healthy individuals above their cognitive best," said Bita Moghaddam, project investigator and professor of neuroscience. "We found that members of this population can enhance their working memory performance even further, despite their already being at the top of their cognitive game."
Led by Rajesh Narendarn, project principal investigator and associate professor of radiology, the Pitt research team sought healthy young men and women from all ethnicities to boost their Omega-3 intake with supplements for six months. They were monitored monthly through phone calls and outpatient procedures. Before they began taking the supplements, all participants underwent positron emission tomography (PET) imaging, and their blood samples were analyzed. They were then asked to perform a working memory test in which they were shown a series of letters and numbers. The young adults had to keep track of what appeared one, two, and three times prior, known as a simple "n-back test."
"What was particularly interesting about the presupplementation n-back test was that it correlated positively with plasma Omega-3," said Moghaddam. "This means that the Omega-3s they were getting from their diet already positively correlated with their working memory."
After six months of taking Lovaza—an Omega-3 supplement approved by the Federal Drug Administration—the participants were asked to complete this series of outpatient procedures again. It was during this last stage, during the working memory test and blood sampling, that the improved working memory of this population was revealed.
"So many of the previous studies have been done with the elderly or people with medical conditions, leaving this unique population of young adults unaddressed," said Matthew Muldoon, project coinvestigator and associate professor of medicine at Pitt. "But what about our highest-functioning periods? Can we help the brain achieve its full potential by adapting our healthy behaviors in our young adult life? We found that we absolutely can."
Although the effects of Omega-3s on young people were a focus, the Pitt team was also hoping to determine the brain mechanism associated with Omega-3 regulation. Previous rodent studies suggested that removing Omega-3 from the diet might reduce dopamine storage (the neurotransmitter associated with mood as well as working memory) and decrease density in the striatal vesicular monoamine transporter type 2 (commonly referred to as VMAT2, a protein associated with decision making). Therefore, the Pitt researchers posited that increasing VMAT2 protein was the mechanism of action that boosted cognitive performance. Unfortunately, PET imaging revealed this was not the case.
"It is really interesting that diets enriched with Omega-3 fatty acid can enhance cognition in highly functional young individuals," said Narendarn. "Nevertheless, it was a bit disappointing that our imaging studies were unable to clarify the mechanisms by which it enhances working memory."
Ongoing animal modeling studies in the Moghaddam lab indicate that brain mechanisms that are affected by Omega-3s may be differently influenced in adolescents and young adults than they are in older adults. With this in mind, the Pitt team will continue to evaluate the effect of Omega-3 fatty acids in this younger population to find the mechanism that improves cognition.
Healthy young adults showed improvements in working memory following omega-3 supplementation in this small experimental study.
Similar findings have already been reported from animal studies and some human trials involving people with memory problems, but improvements in 'normal' healthy people would indeed be a noteworthy finding.
Because this was not a randomised controlled trial (RCT), the 'treatment effects' reported here do need to be viewed with caution. However, similar benefits of omega-3 supplementation for working memory in healthy young adults have already been demonstrated in a much larger and very rigorously conducted RCT carried out in New Zealand. These results were presented at scientific conferences earlier this year (Stonehouse et al, May 2012, ISSFAL Vancouver, and Conlon et al, July 2012, Massey University, Auckland, NZ) and have received some media coverage, although full publication is still awaited.
A primary purpose of the new study reported here was to investigate possible mechanisms - specifically, dopamine receptor density in brain regions important for working memory.
Blood omega-3 status and working memory were significantly associated with each other at the pre-treatment baseline, but although both improved following supplementation, the changes were not correlated with changes in brain dopamine receptors as assessed here via brain imaging.
This suggests either that effects of omega-3 on working memory were operating through other mechanisms, or that the measures were not sufficiently sensitive in such a small sample. Nonetheless, this study makes an important contribution in showing that blood omega-3 status predicted cognitive performance in healthy young adults, and in finding apparent benefits of omega-3 supplementation for working memory.
Full details of the study are freely available online: see
3279Torres-Vega et al 2012 - Limbic system pathologies associated with deficiencies and excesses of the trace elements iron, zinc, copper, and seleniumLimbic system pathologies associated with deficiencies and excesses of the trace elements iron, zinc, copper, and seleniumLimbic system pathologies associated with deficiencies and excesses of the trace elements iron, zinc, copper, and seleniumTorres-Vega A, Pliego-Rivero BF, Otero-Ojeda GA, Gómez-Oliván LM, Vieyra-Reyes P.25/10/2012Nutr Rev70(12)679-92. Epub 2012 Oct 25.
Deficiencies of nutrients such as amino acids, vitamins, lipids, and trace elements during gestation and early infanthood have strong deleterious effects on the development of the limbic system; these effects may be irreversible, even when adequate supplementation is provided at later developmental stages.
Recent advances in the neurochemistry of biometals are increasingly establishing the roles of the trace elements iron, copper,zinc, and selenium in a variety of cell functions and are providing insight into the repercussions of deficiencies and excesses of these elements on the development of the central nervous system, especially the limbic system.
The limbic system comprises diverse areas with high metabolic demands and differential storage of iron, copper, zinc, and selenium. This review summarizes available evidence suggesting the involvement of these trace elements in pathological disorders of the limbic system.
iron, zinc, copper, selenium, limbic system, brain development, brain function, emotional processing, arousal, neurotransmitter function, depression, ADHD, epilepsy, Alzheimer's disease, dementia, Parkinson's disease, Huntington's disease, schizophrenia, neurological disorders, psychiatric disorders, animal studies, human studies, reviewhttp://www.ncbi.nlm.nih.gov/pubmed/23206282View this and related abstracts via PubMed here
3183Andreeva et al 2012 - Supplementation with B vitamins or n-3 fatty acids and depressive symptoms in cardiovascular disease survivors.Supplementation with B vitamins or n-3 fatty acids and depressive symptoms in cardiovascular disease survivors: ancillary findings from the SUpplementation with FOLate, vitamins B-6 and B-12 and/or OMega-3 fatty acids (SU.FOL.OM3) randomized trial.Supplementation with B vitamins or n-3 fatty acids and depressive symptoms in cardiovascular disease survivors: ancillary findings from the SUpplementation with FOLate, vitamins B-6 and B-12 and/or OMega-3 fatty acids (SU.FOL.OM3) randomized trial.Andreeva VA, Galan P, Torrès M, Julia C, Hercberg S, Kesse-Guyot E.24/10/2012Am J Clin Nutr. 96(1)208-14. Epub 2012 May 30.
OBJECTIVE: In secondary data analyses, we examined effects of supplementation with B vitamins or n-3 (omega-3) fatty acids on depressive symptoms in cardiovascular disease survivors.
DESIGN: The SUpplementation with FOLate, vitamins B-6 and B-12 and/or OMega-3 fatty acids (SU.FOL.OM3) trial was a secondary prevention trial (2003-2009; n = 2501) in which individuals aged 45-80 y were randomly assigned, by using a 2 × 2 factorial design, to receive 0.56 mg 5-methyl-tetrahydrofolate and vitamins B-6 (3 mg) and B-12 (0.02 mg); EPA and DHA (600 mg) in a 2:1 ratio; B vitamins and n-3 fatty acids; or a placebo. Depressive symptoms were evaluated at years 3 and 5 with the 30-item Geriatric Depression Scale (GDS). Overall and sex-specific ORs and 95% CIs were estimated in 2000 participants by using factorial logistic regression.
RESULTS: After a median of 4.7 y of supplementation, there was no association between allocation to receive B vitamins and depressive symptoms. However, the allocation to receive n-3 fatty acids was positively associated with depressive symptoms (GDS >10) in men (adjusted OR: 1.28; 95% CI: 1.03, 1.61) but not in women.
CONCLUSIONS: We showed no beneficial effects of a long-term, low-dose supplementation with B vitamins or n-3 fatty acids on depressive symptoms in cardiovascular disease survivors. The adverse effects of n-3 fatty acids in men merit confirmation.
omega-3, B vitamins, vitamin_B6, vitamin_B12, depression, cardiovascular disease, human study, RCThttp://www.ncbi.nlm.nih.gov/pubmed/22648722View this and related abstracts via PubMed here.
3487Tammam J et al 2012 - Availability of junk food should be reducedAvailability of junk food should be reducedAvailability of junk food should be reducedTammam J, Gillam L, Gesch B, Stein J.24/10/2012BMJ 2012;345:e7070
Prison inmates rely on two sources of food—main meals (provided by the prison) and items purchased from the canteen, the penal equivalent of a convenience store.
Prison meals meet nutritional guidelines, but purchased items—much of it “junk” food—may not. We analysed macronutrient and energy content of food available in a canteen from …
prison food; junk food; anti-social behaviourhttp://www.bmj.com/content/345/bmj.e7070View the abstract and access full paper at BMJ online here
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